The Experts below are selected from a list of 189 Experts worldwide ranked by ideXlab platform
John E. Hall - One of the best experts on this subject based on the ideXlab platform.
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Chronic antidiabetic and cardiovascular actions of leptin: role of CNS and increased Adrenergic Activity
American journal of physiology. Regulatory integrative and comparative physiology, 2006Co-Authors: Alexandre A. Da Silva, Lakshmi S. Tallam, Jiankang Liu, John E. HallAbstract:This study examined the importance of direct central nervous system (CNS) actions and increased Adrenergic Activity in mediating the chronic antidiabetic and cardiovascular actions of leptin. Insul...
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Chronic Cardiovascular and Renal Actions of Leptin: Role of Adrenergic Activity
Hypertension, 2002Co-Authors: Megan Carlyle, Oscar B. Jones, Jay J. Kuo, John E. HallAbstract:Abstract— This study was designed to determine the role of changes in Adrenergic Activity in mediating the chronic cardiovascular, renal, and metabolic actions of leptin. Male Sprague-Dawley rats were implanted with catheters for mean arterial pressure (MAP) and heart rate (HR) measurements and IV infusions of either vehicle (n= 7) or α- and β-Adrenergic receptor antagonists, terazosin and propranolol (10 mg/kg/d; n= 8) throughout the study. After control measurements, murine leptin was infused IV (1.0 μg/kg/min) for 7 days along with vehicle or Adrenergic antagonists, followed by a 7-day recovery period. Leptin infusion significantly reduced food intake in control rats from 22.6±0.8 to 10.6±0.4 g/d and, in Adrenergic blockade rats, from 22.6±0.8 to 13.2±0.8 g/d. Fasting plasma insulin decreased from 48±10 to 5±2 μU/mL in control rats and from 51±9 to 9±2 μU/mL in Adrenergic blockade rats during leptin infusion. Leptin infusion did not significantly alter glomerular filtration rate in either group. MAP and HR increased by 6±1 mm Hg and 23±7 bpm after 7 days of leptin infusion in control rats. However, in Adrenergic blockade rats, leptin infusion did not significantly alter MAP (−1±1 mm Hg) and decreased, rather than increased, HR (−23±8 bpm). These results indicate that leptin-induced increases in blood pressure and tachycardia are mediated by increased Adrenergic Activity and support the concept that leptin may be an important link between obesity, increased sympathetic Activity, and hypertension. However, the chronic effects of leptin on insulin and glucose regulation do not appear to be altered by α- and β-Adrenergic receptor blockade.
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Chronic cardiovascular and renal actions of leptin: role of Adrenergic Activity.
Hypertension (Dallas Tex. : 1979), 2002Co-Authors: Megan Carlyle, Oscar B. Jones, Jay J. Kuo, John E. HallAbstract:This study was designed to determine the role of changes in Adrenergic Activity in mediating the chronic cardiovascular, renal, and metabolic actions of leptin. Male Sprague-Dawley rats were implanted with catheters for mean arterial pressure (MAP) and heart rate (HR) measurements and IV infusions of either vehicle (n= 7) or alpha- and beta-Adrenergic receptor antagonists, terazosin and propranolol (10 mg/kg/d; n= 8) throughout the study. After control measurements, murine leptin was infused IV (1.0 microg/kg/min) for 7 days along with vehicle or Adrenergic antagonists, followed by a 7-day recovery period. Leptin infusion significantly reduced food intake in control rats from 22.6 +/- 0.8 to 10.6 +/- 0.4 g/d and, in Adrenergic blockade rats, from 22.6 +/- 0.8 to 13.2 +/- 0.8 g/d. Fasting plasma insulin decreased from 48 +/- 10 to 5 +/- 2 microU/mL in control rats and from 51+/- 9 to 9 +/- 2 microU/mL in Adrenergic blockade rats during leptin infusion. Leptin infusion did not significantly alter glomerular filtration rate in either group. MAP and HR increased by 6 +/- 1 mm Hg and 23 +/- 7 bpm after 7 days of leptin infusion in control rats. However, in Adrenergic blockade rats, leptin infusion did not significantly alter MAP (-1 +/- 1 mm Hg) and decreased, rather than increased, HR (-23 +/- 8 bpm). These results indicate that leptin-induced increases in blood pressure and tachycardia are mediated by increased Adrenergic Activity and support the concept that leptin may be an important link between obesity, increased sympathetic Activity, and hypertension. However, the chronic effects of leptin on insulin and glucose regulation do not appear to be altered by alpha- and beta-Adrenergic receptor blockade.
John G.f. Cleland - One of the best experts on this subject based on the ideXlab platform.
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The Control of Adrenergic Function in Heart Failure: Therapeutic Intervention
Heart Failure Reviews, 2000Co-Authors: Andrew L. Clark, John G.f. ClelandAbstract:Chronic heart failure is characterised by excess Adrenergic Activity that augurs a poor prognosis. The reasons for increased Adrenergic Activity are complex and incompletely understood. The circumstantial evidence relating increased Activity to adverse outcome is powerful, but not yet conclusive. In normal subjects, autonomic control of the circulation is predominantly under the control of sympatho-inhibitory inputs from the arterial and cardiopulmonary baroreceptors, with a small input from the excitatory ergo- and chemo-receptors. In heart failure, the situation is reversed, with loss of the restraining input from the baroreceptors and an increase in the excitatory inputs, resulting in excessive Adrenergic Activity. The circumstantial evidence linking neuroendocrine activation with poor outcome coupled with the clinical success of inhibition of the renin-angiotensin-aldosterone system has long suggested that inhibition of Adrenergic Activity might be beneficial in heart failure. There is a number of potential ways of achieving this. Improved treatment of heart failure itself may reduce sympathetic drive. There is an interplay between angiotensin II, aldosterone and the sympathetic nervous system, and thus RAAS antagonists, such as angiotensin converting enzyme inhibitors and spironolactone could directly reduce sympathetic activation. Exercise rehabilitation may similarly reduce sympathetic Activity. Recently, β-Adrenergic receptor antagonists have been conclusively shown to improve symptoms, reduce hospitalisations and increase survival. However, the demonstration that central reduction of sympathetic Activity with agents such as moxonidine increases morbidity and mortality suggests that we do not properly understand the role of sympathetic activation in the pathophysiology of heart failure.
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The control of Adrenergic function in heart failure: therapeutic intervention.
Heart failure reviews, 2000Co-Authors: Andrew L. Clark, John G.f. ClelandAbstract:Chronic heart failure is characterised by excess Adrenergic Activity that augurs a poor prognosis. The reasons for increased Adrenergic Activity are complex and incompletely understood. The circumstantial evidence relating increased Activity to adverse outcome is powerful, but not yet conclusive.
Steven K. Krueger - One of the best experts on this subject based on the ideXlab platform.
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effect of baseline or changes in Adrenergic Activity on clinical outcomes in the β blocker evaluation of survival trial
Circulation, 2004Co-Authors: Michael R. Bristow, R. Nuzzo, Cheng Seng Liang, Joann Lindenfeld, Brian D. Lowes, Brack Hattler, William T. Abraham, L. Olson, Steven K. Krueger, Heidi KrausesteinraufAbstract:Background— Adrenergic activation is thought to be an important determinant of outcome in subjects with chronic heart failure (CHF), but baseline or serial changes in Adrenergic Activity have not been previously investigated in a large patient sample treated with a powerful antiAdrenergic agent. Methods and Results— Systemic venous norepinephrine was measured at baseline, 3 months, and 12 months in the β-Blocker Evaluation of Survival Trial (BEST), which compared placebo treatment with the β-blocker/sympatholytic agent bucindolol. Baseline norepinephrine level was associated with a progressive increase in rates of death or death plus CHF hospitalization that was independent of treatment group. On multivariate analysis, baseline norepinephrine was also a highly significant (P<0.001) independent predictor of death. In contrast, the relation of the change in norepinephrine at 3 months to subsequent clinical outcomes was complex and treatment group-dependent. In the placebo-treated group but not in the bucind...
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Effect of Baseline or Changes in Adrenergic Activity on Clinical Outcomes in the β-Blocker Evaluation of Survival Trial
Circulation, 2004Co-Authors: Michael R. Bristow, Heidi Krause-steinrauf, R. Nuzzo, Cheng Seng Liang, Joann Lindenfeld, Brian D. Lowes, Brack Hattler, William T. Abraham, L. Olson, Steven K. KruegerAbstract:Background— Adrenergic activation is thought to be an important determinant of outcome in subjects with chronic heart failure (CHF), but baseline or serial changes in Adrenergic Activity have not been previously investigated in a large patient sample treated with a powerful antiAdrenergic agent. Methods and Results— Systemic venous norepinephrine was measured at baseline, 3 months, and 12 months in the β-Blocker Evaluation of Survival Trial (BEST), which compared placebo treatment with the β-blocker/sympatholytic agent bucindolol. Baseline norepinephrine level was associated with a progressive increase in rates of death or death plus CHF hospitalization that was independent of treatment group. On multivariate analysis, baseline norepinephrine was also a highly significant (P
Karin Roelofs - One of the best experts on this subject based on the ideXlab platform.
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Cortisol-induced impairments of working memory require acute sympathetic activation.
Behavioral neuroscience, 2005Co-Authors: Bernet M. Elzinga, Karin RoelofsAbstract:The present study assessed whether the effects of cortisol on working memory depend on the level of Adrenergic Activity (as measured by sympathetic activation) during memory performance. After exposure to a psychosocial stress task, participants were divided into cortisol responders and nonresponders. Cortisol responders showed working memory impairments during the psychosocial stress phase, when cortisol and Adrenergic Activity were enhanced, whereas nonresponders did not. During recovery, however, when cortisol levels were elevated but Adrenergic Activity was normalized, working memory of responders did not differ from that of nonresponders. Among several stress measures, cortisol was the only significant predictor for working memory performance during stress. These findings suggest that Adrenergic activation is essential for the impairing effects of stress-induced cortisol on working memory.
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Behavioral Neuroscience - Cortisol-induced impairments of working memory require acute sympathetic activation.
Behavioral neuroscience, 2005Co-Authors: Bernet M. Elzinga, Karin RoelofsAbstract:The present study assessed whether the effects of cortisol on working memory depend on the level of Adrenergic Activity (as measured by sympathetic activation) during memory performance. After exposure to a psychosocial stress task, participants were divided into cortisol responders and nonresponders. Cortisol responders showed working memory impairments during the psychosocial stress phase, when cortisol and Adrenergic Activity were enhanced, whereas nonresponders did not. During recovery, however, when cortisol levels were elevated but Adrenergic Activity was normalized, working memory of responders did not differ from that of nonresponders. Among several stress measures, cortisol was the only significant predictor for working memory performance during stress. These findings suggest that Adrenergic activation is essential for the impairing effects of stress-induced cortisol on working memory.
Andrew L. Clark - One of the best experts on this subject based on the ideXlab platform.
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The Control of Adrenergic Function in Heart Failure: Therapeutic Intervention
Heart Failure Reviews, 2000Co-Authors: Andrew L. Clark, John G.f. ClelandAbstract:Chronic heart failure is characterised by excess Adrenergic Activity that augurs a poor prognosis. The reasons for increased Adrenergic Activity are complex and incompletely understood. The circumstantial evidence relating increased Activity to adverse outcome is powerful, but not yet conclusive. In normal subjects, autonomic control of the circulation is predominantly under the control of sympatho-inhibitory inputs from the arterial and cardiopulmonary baroreceptors, with a small input from the excitatory ergo- and chemo-receptors. In heart failure, the situation is reversed, with loss of the restraining input from the baroreceptors and an increase in the excitatory inputs, resulting in excessive Adrenergic Activity. The circumstantial evidence linking neuroendocrine activation with poor outcome coupled with the clinical success of inhibition of the renin-angiotensin-aldosterone system has long suggested that inhibition of Adrenergic Activity might be beneficial in heart failure. There is a number of potential ways of achieving this. Improved treatment of heart failure itself may reduce sympathetic drive. There is an interplay between angiotensin II, aldosterone and the sympathetic nervous system, and thus RAAS antagonists, such as angiotensin converting enzyme inhibitors and spironolactone could directly reduce sympathetic activation. Exercise rehabilitation may similarly reduce sympathetic Activity. Recently, β-Adrenergic receptor antagonists have been conclusively shown to improve symptoms, reduce hospitalisations and increase survival. However, the demonstration that central reduction of sympathetic Activity with agents such as moxonidine increases morbidity and mortality suggests that we do not properly understand the role of sympathetic activation in the pathophysiology of heart failure.
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The control of Adrenergic function in heart failure: therapeutic intervention.
Heart failure reviews, 2000Co-Authors: Andrew L. Clark, John G.f. ClelandAbstract:Chronic heart failure is characterised by excess Adrenergic Activity that augurs a poor prognosis. The reasons for increased Adrenergic Activity are complex and incompletely understood. The circumstantial evidence relating increased Activity to adverse outcome is powerful, but not yet conclusive.
